Problem Set Key Points Flashcards
Central DI - typical findings?
low ADH production -> water wasting
high serum Na (hypernatremia)
urine osms is inappropriately low (due to dilution)
low BP, high HR
Central DI - expected aldosterone?
evidence of this?
elevated aldosterone
low FENa
Urine Na is low
Central DI - ECV?
low
Central DI - sx if patient is awake? unconscious?
awake - polyuria + polydipsia
unconscious - hypernatremia
water deficit eqn?
wt (0.6) * (actual Na/140 - 1)
Central DI trmt? 3
1) desmopressin
2) NS or 5% dextrose to normalize BP/HR
3) drink water
Central DI with normotremia? How is it possible?
conscious person drinks water
excessive sweating + lack of water intake causes:
body’s response?
trmt? 2
loss of H2O + Na -> decreased ECV
response to incr. aldosterone -> incr. K/H loss, Na retention -> high Na
trmt:
1) isotonic saline to restore ECV
2) electrolytes or D5W with KCl to replace K
excessive sweating + excess water intake causes:
body’s response?
trmt? 2
excess sweating -> decr. ECV
response: incr. ADH levels/thirst; drinking water causes fluids to distribute in all compartments (so even if they’re in fluid excess, their ECV is low.
trmt:
1) isotonic saline with K to restore ECV
2) ORT to restore ECV
once ECV is normalized, ADH decreases, enabling diuresis.
SIADH - evidence?
BP elevated
Na is low (hyponatremia due to xs water retention)
Urine Osms»_space; serum Osms
SIADH - aldosterone levels?
usually normal (remember SIADH patients are euvolemic because they have reduced AII, which is a driver of thirst)
SIADH - treatment if patient has no sx? with sx?
no sx: H2O restriction
with sx: hypertonic Na
SIADH - what happens if patient is given NS?
patient retains H2O because body can’t dilute his urine, worsens hyponatremia
Nephrotic syndrome - characterized by? 2
what does it result in?
How does it affect: total body water content: total body Na content ECFV ECV urine Na excretion urine osmolarity
trmt? 4
leaky capillaries + low serum albumin –> loss of intravascular fluid volume to interstitial space –> edema + decr. ECV
results in RAAS activation + ADH + thirst
total body water content: high total body Na content: high ECFV: high ECV: low urine Na excretion: low urine osmolarity: high
trmt:
1) restrict Na to minimize edema
2) colloid (IV albumin) to improve intravascular volume
3) restrict fluids
4) steroids or bx
ESRD - causes
what is a patient usually on if they have ESRD?
trmt if a patient overloads with beer + soft drinks? 3
will giving hypertonic saline work? Why/Why not?
decr. free H2o excretion
usually on dialysis
trmt:
1) fluid restriction
2) restrict Na - bc this incr. plasma osmolarity + thirst
2) dialysis
hypertonic saline won’t work because patient is already on dialysis. Giving him that much saline will result in
- edema, HTN, pulmonary edema
Why? Na distributes to extracellular space, leads to H2O retention -> increased hydrostatic pressures –> edema
beer potomania - what does it cause?
evidence of this?
trmt? 1
What should you do if the patient refuses to listen to your treatment?
hyponatremia
evidence: alcoholic, urine is maximally dilute (since pt usually has insufficient osmoles available to produce enough urine to excrete the excess H2O)
Trmt:
1) restrict osmolar intake - bc ADH is completely suppressed already and any osmolar intake will be excreted in very dilute urine to remove free H2O. If this happens too fast –> central pontine demyelination
2) if osmolar intake is increased, provide free H2O or ddvap to slow the rate of correction.
Poor patient on HCTZ with
- poorly controlled BP
- K = 2.5meq/l
- HCO3 = 30meq/l
what caused hypokalemia? 4
Hypokalemia sx: 4
1a) hctz -> incr. Na delivered distally -> K excretion
1b) hctz -> decr. ECV -> 2˚ hyperaldosteronism
2) poor - isn’t eating right
3) RAS or 1˚ hypoaldsteronism due to HTN + hypokalemia (severe)
4) alkalotic state -> HCO3 excretion -> provides (-) charge that is favors K secretion
Hypokalemia sx
1) fatigue
2) palpitations
3) muscle weakness
4) metabolic alkalosis - due to decr. renal perfusion due to thiazide-induced volume depletion AND hypokalemia (K leaves cells, H enters cells)
trmt for hypokalemia caused by hctz diuretic
1) KCl supplements
2) K sparing diuretics (ACEi/ARBs), ß blockers, Ca channel blockers
3) diuretics + KCl supplements
Pt. with BPH; labs show
- 7.0meq/l K
- 8.0mg/dL Ca
trmt plan? 3
ddx of low k? 4
How does BPH affect his situation?
lab/studies to order?
1) EKG
2) IV Ca to stabilize myocardium and decr. risk of arrhythmias and cardiac arrest
3) decr. K with: dextrose + insulin, ß agonist, kayexylate
ddx:
- incr. intake
- decr. excretion (k sparing diuretics, decr. GFR, hypoaldosteronism)
- transcellular shift - high osmolar states, hypoinsulin, acidosis, cell lysis, GI bleed
- spurious
BPH - obstruction -> acute kidney injury and ischemia due to back pressure (type IV RTA)
order labs to r/o causes of his hyperkalemia:
1) serum creatinine to test renal fxn
2) blood glucose to r/o hypoinsulinemia
3) ABG to r/o acidosis
4) US of kidney and bladder
4yo lethargy, incr. urine output, very thirsty. labs:
- low BP
- dry mucous membranes
- rapid deep breaths
- Na = 130
- K = 6.5
- Cl = 96
- HCO3 = 5
- glucose = 450
- creatinine = 1.2
- BUN - 25
What’s her AG?
Dx?
Causes of hyperkalemia in this 4yo? 4
Causes of hyponatremia in this 4yo? 3
trmt? 3
AG = 29
Dx: DKA
causes of hyperkalemia
1) acidosis
2) decr. insulin levels
3) hyperosmolarity -> causes H2O to leave the cell
4) decr. GFR
Hyponatremia causes?
1) intracellular shift of H2O to EC space
2) incr ADH due to decr ECV
3) xs thirst
trmt:
1) insulin
2) KCl cotreatment
3) Phosphate cotreatment (glucose moves into cells and is phosphorylated)
Why must you cotreat with KCl in a patient with DKA?
underlying total body K deficit
developed during the earlier phase of the DKA due to decreased oral intake, osmotic diuresis (polyuria) and increased aldosterone level due to decr. ECV
Approach to A/B problem? 3
1) calculate anion gap to determine if its AG acidosis or hyperchloremic acidosis
2) calculate expected CO2 (winter’s formula) to determine if there is compensation
3) calculate UAG to determine if there is appropriate renal compensation - esp. if urine values are provided!!
What should you think of when you see a patient with chronic diarrhea?
HYPERCHLOREMIC ACIDOSIS (WITH NORMAL AG)
Winter’s formula?
1.5*HCO3 + 8
If you see this electrolyte profile in urine, what should you think of?
Na 77 mEq/L, K 43 mEq/L, Cl 52 mEq/L
lasix (furosemide) abuse
Net electrolyte effects of starvation
decr. glucose -> decr. insulin -> hyperkalemia
Net effects of laxatives (2)
HCO3 loss -> metabolic acidosis
decr. ECV -> RAAS -> incr. aldo -> Na uptake/K secretion
Net effects of lasix diuretic: (2)
Na, K, Cl loss (Na is lost, HCO3 is not reabsorbed)
decr. ECV -> RAAS -> incr. aldo -> Na uptake/K secretion
Net effects of vomiting: (2)
HCl loss -> metabolic alkalosis w. hypokalemia (HCO3 excretion draws K out into lumen for charge balance)
decr. ECV -> RAAS -> incr. aldo -> Na uptake/K secretion
How can you tell if someone is abusing lasix diuretics?
measure lasix in the urine
What does this profile tell you?
Na+ 126 mEq/L, K+ 2.7 mEq/L, Cl- 88 mEq/L, HCO3- 32 mEq/L, BUN 34 mg/dL, Cr 0.8 mg/dL, glucose 80 mg/dL
ABG: pH 7.44, pCO2 47 mmHg, pO2 100 mmHg
metabolic alkalosis w. respiratory compensation
difference between Barrter’s and Gitelmans?
urine calcium
- Bartter’s- furosemide(loop)-like; elevated
- Gitelman’s - thiazide-like; normal
elevated anion gap metabolic acidosis + concomitant respiratory alkalosis
dx?
salicylate poisoning
patient tells you “I am taking pain medication and have tinnitus”
what is he taking?
What should you expect his labs to be?
salicylate
elevated anion gap metabolic acidosis + concomitant respiratory alkalosis
utility of serum osmolality?
may reveal evidence of other ingestion if difference between calculated vs. actual is >10.
think MUDPILES for incr. osmolar gap with acidosis
think LIMP-LED for incr. osmolar gap w/o acidosis
causes of incr. osmolar gap with acidosis?
causes of incr. osmolar gap w/o acidosis?
think MUDPILES for incr. osmolar gap with acidosis (methanol, uremia, DKA, paraldehyde, INH, lactic acidosis, ethylene glycol, salicyclates)
think LIMP-LED for incr. osmolar gap w/o acidosis (lithium, isopropanol, mannitol, protein, lipid, ethanol, diethyl ether)
Unresponsive man who is frequently intoxicated had urinalysis: SG 1.025, pH 5, 1+ protein, 3+ blood, positive fluorescence under UV light. Stats were:
Na+ 144 mEq/L, K+ 6.4 mEq/L, Cl- 102 mEq/L, HCO3- 14 mEq/L, BUN 30 mg/dL, Cr 2.5 mg/dL, glucose 90 mg/dL
ABG: pH 7.34, pCO2 30 mmHg, pO2 100 mmHg
What is the acid/base status?
What is AG?
Osmolar gap?
What was his status before he had ingested the toxin?
met acidosis w. respiratory compensation (appropriate because winters calculation gives expected CO2 of 29)
AG = 28 = AG acidosis
therefore he has a MIXED d/o
Osmolar gap = 17
AG is elevated by 16 from normal; and chemically, this should consume 16 mEq/L of HCO3, leading to a serum HCO3 of 8 if he had started off a normal bicarb of 24. BUT he had a HCO3 of 14, indicating that he had a started off with a HCO3 of 30.
His ∆∆ is 16-10 = 6, which indicates that he had a concomitant metabolic alkalosis. The patient is likely volume depleted, either from vomiting or lack of fluid intake in his obtunded state
∆AG = 28-12 = 16
∆HCO3 = 24-14 = 10
Patient with BPH - what is the cause of renal failure?
What would you see on US? (3)
Metabolic abnormalities?
Trmt? (2)
post-renal obstruction back-pressure -> hypoperfusion of the medulla, which impairs the ability of the kidney to concentrate the urine in the collecting duct.
US: hydronephrosis, distended bladder, enlarged prostate
Metabolic abnormalities:
1) Type IV RTA: hyperkalemia + non-AG metabolic acidosis
2) dilute urine - due to impaired concententrating ability
Trmt:
1) catheter to relieve obstruction slowly to avoid
- venous plexus damage (bleeding)
- high volume diuresis (hypokalemia + hypoMg)
2) replace K/Mg as needed
4yo with vomiting+diarrhea - what is the cause of his renal failure?
Metabolic abnormalities? (3)
Trmt? (2)
pre-renal: decr. in ECV due to volume losses from diarrhea + vomiting
Metabolic abnormalities
1) hyponatremia - ADH-mediated uptake of H2O
2) hypokalemia - excess HCO3 secretion (- charge) favors K secretion, also, aldosterone mediated Na uptake/K secretion
3) met. alkalosis - vomiting -> excess HCO3
Trmt: NS to restore ECV
52yo with sx of CHF (pleural effusion + edema) - what is the cause of his renal failure?
labs?
What is meaning of FENa is 0.49?
He has high urine osmolarity and low Na = indications?
He has hyponatremia. Why is that?
He is hypOkalemic. Why is that?
He has decreased serum HCO3. What d/o must be present? What should you calculate to prove this?
Why is it possible that he can present with hypERkalemia? (2)
Trmt?
pre-renal: CHF-induced decrease ECV -> decr. GFR
- activated sympathetics, RAAS, ADH
- incr. BUN+creatinine
FENa 0.49 = kidneys are functioning properly to reabsorb H2O
incr. urine osm + low Na = due to ADH reabsorption of water + AII/Aldo reabsorption of Na, but the combination of these two signal increased risk of ATN
Hyponatremia = decreased ECV -> incr. ADH + thirst -> too much H2O
Hypokalemic = incr. aldosterone
d/o:
1) respiratory alkalosis - stiff lungs stimulate respiratory drive
2) decr. CO -> incr. accumulation of LACTIC ACIDOSIS due to decreased tissue perfusion and accumulation of UREMIA toxins from renal failure.
Calculate AG = 21 - indication that there’s an unaccounted anion present
Hyperkalemic = 1) decr. renal perfusion -> decr. distal Na delivery -> no Na to exchange for K
2) ACEi/ARB use -> type IV RTA -> hyperkalemia
Trmt: Improve cardiac flow - ionotropes, diuretics, vasodilators to reduce afterload on the heart.
Woman treated with gentamicin for 8 days and saw creatinine rise to 5.2. Cause of renal failure?
Prognosis?
Tubular-interstitial toxicity (intrinsic) renal failure: gentamicin is an aminoglycoside that can affect mitochondrial function and IP3 signaling in the proximal RTE cells.
Prognosis: generally good because RTE cells can be repopulated from stem cells
24yo with crush injury and no access to food/water for 2 days. Cause of his renal failure?
Urine color and why?
expected urine Na levels and FENa?
Other substances that can cause same mxn of renal toxicity? (4)
if he remains anuric, what is expected to happen to his serum creatinine?
Trmt? 3
Tubulointerstitial injury (intrinsic) renal failure - due to myoglobin, which
- causes afferent arteriole vasoconstriction
- direct toxicity to RTE
urine color = red because myoglobin is small enough to be filtered through
Urine Na levels = low due to incr. AII/Aldo
FENA = low due to afferent arteriole vasoconstriction
similar substances
1) iodinated contrast
2) massive hemolysis
3) NSAIDs
4) Calcineurin inhibitors
creatinine: rise
Trmt:
1) hydration
2) alkalinzation to increase myoglobin solubility
3) dialysis if there is evidence of renal failure
9yo with low-grade fevers with decr. PO intake 2 weeks ago. Currently presents with brown-colored urine, 1+ edema, BP 162/98.
Labs: Na=140, Cl =105, HCO3=22, K=5.2, creatinine =2.2
Urinalysis shows 2+ protein, RBC+casts.
What form of renal failure does he have? BE SPECIFIC
Why is he edematous even though proteinuria is not that high?
treatment? 2
intrinsic renal failure due to glomerulonephritis
- likely PIGN - nephritic presentation because of his hematuria, proteinuria, HTN, and edema
edematous because of fluid overload as a result of decr. GFR + Na retention (due to RAAS activation)
trmt:
1) restrict fluid, Na, K to avoid worsening overload/edema
2) BP control
What does a low urine Na + high urine osm suggest?
decreased ECV
what does high urine osm suggest?
ADH is present or ADH activity
What does a high urine osm + high urine Na suggest?
physiologically inappropriate ADH = SIADH
how do you distinguish between 1˚ polydipsia and beer potomania?
total urine volume or total fluid intake - otherwise they look the same.
(1˚ polydipsia = urine volume >15L)
A 70 year-old man presents to the ED with weakness. He is on no medications. Physical examination reveals a well nourished male in no distress. Vital signs: P 70, BP 120/80, R 12. Head and neck examination are unremarkable. JVP is 5cm H2O. Lungs are clear, heart is regular without murmurs, and there is no peripheral edema.
Labs: Na 120, K 4.0, Cl 84, HCO3 24, BUN 6, Cr 0.7 Serum osms 250 Urine osms 600 Urine Na 60, Urine Cr 20
What is the most likely etiology of his hyponatremia?
A. Hyperglycemia
B. Decreased effective circulating volume
C. Primary Polydipsia
D. SIADH
E. Low osmolar intake (beer potomania / “tea and toast” syndrome)
D. SIADH
Pt is euvolemic by examination and vital signs and has hyposomolar hyponatremia.
NOT hyperglycemia b/c serum osmolarity is low
NOT ECV because urine Na is not low
NOT primary polydipsia or low osmolar intake (water intake»osmoles available to excrete it) because the urine osms are high
A 75 year-old woman presents to the ED with fatigue. She is not taking medications. Physical examination reveals a thin female in no distress. Vital signs: P 80, BP 100/60 without postural changes, R 14. Head and neck examination are normal. JVP is 4 cm H2O. Lungs are clear to auscultation, cardiac examination is normal, no peripheral edema.
Labs:
Na 120, K 4.0, Cl 84, HCO3 24, BUN 4, Cr 0.4
Serum osms 250
Urine osms 50
Urine Na 15
24 hour urine collection: total volume 2L, total osms 100
What is the most likely etiology of her hyponatremia?
A. Hyperglycemia
B. Decreased effective circulating volume
C. Primary Polydipsia
D. SIADH
E. Low osmolar intake (beer potomania / “tea and toast” syndrome)
E. low osmolar intake (beer potomania / “tea and toast” syndrome)
Pt is euvolemic and hypoosmolar.
Serum sodium is low and the urine is maximally diluted so water intake»_space; available osmoles for excretion.
The low total urine volume rules out primary polydipsia.
A patient with bipolar disorder on lithium therapy presents with polyuria, thirst, diarrhea, vomiting, and fatigue. Labs show: Na 150, K 3.0, Cl 110, CO2 28, BUN 30, Cr 1.4, Urine Na 20, Urine osms 800.
Which of the following is the most likely etiology of his hypernatremia? A. Central diabetes insipidus B. Nephrogenic diabetes insipidus C. Diabetes mellitus D. GI fluid losses E. Surreptitious furosemide use
C. Diabetes mellitus - hyperglycemia, as seen in diabetes mellitus, can cause an osmotic diuresis, leading to the high urine osms.
Patients are also volume depleted but are unable to maximally remove sodium from the urine as the osmotic diuresis moves urine through the tubule too quickly to reabsorb all the sodium (hence a urine sodium of 20, in between maximal reabsorption and a natriuretic state).
NOT DI (central or nephrogenic) - has very dilute urine GI fluid losses - volume depletion and a very low urine sodium ( 40).
When treating hyponatremia, administration of KCl can raise the serum sodium. How does this occur?
K enters the cells, increasing intracellular osmolarity. Water shifts from the extracellular to intracellular spaces following its osmotic gradient. As water leaves the extracellular space, serum sodium concentration rises.
Patient with oliguric acute renal failure due to extensive blood loss from surgery earlier that day. Serum electrolytes:
Na 135 mEq/l K 6.8 mEq/l Cl 104 mEq/l HCO3 10 mEq/l Arterial pH 7.12 Arterial pCO2 26 mmHg Arterial pO2 120 mmHg. Urine volume 50 mEq/L)
What would you predict the fractional excretion of sodium to be? (2%)
1) decreased GFR (less filtration of K+ leads to decreased excretion)
2) Metabolic acidosis (H+ enters cells, K+ leaves)
3) Decreased distal delivery of Na+ (less available to be reabsorbed and create a - electrical gradient for K+ excretion)
4) Slow tubular flow (K+ accumulates in the tubular lumen, decreasing the chemical gradient for K+ excretion)
5) Resorption of RBC or necrotic tissue can also be seen postoperatively and lead to hyperkalemia.
Urinary Na
A 35-year-old man presents to the emergency room after several days of severe vomiting. Serum electrolytes are as follows: Na 148 mEq/l, K 2.3 mEq/l, Cl 108 mEq/l, HCO3 36 mEq/l
a. What would you predict is the acid-base status of the blood in this patient?
b. What further information would you need to confirm this?
c. How has this acid-base disturbance arisen?
d. List 4 factors contributing to hypokalemia in this patient?
Metabolic alkalosis.
ABG or serum pH
(Primary) metabolic alkalosis (due to vomiting) - loss of HCl
Hypokalemia
1) Decreased K+ intake
2) Met. alkalosis causes intracellular K+ shifts
3) Increased aldosterone due to volume depletion leads to increased urinary loss of K
4) Increased HCO3- at CCD is a non reabsorbable anion that increases the electrochemical gradient for K+ secretion in the distal tubule
5) some loss of K+ in the vomitus, but this is less important quantitatively than the other factors.
A 17-yo male presents to the ED with 2 days of vomiting, weakness, and frequent urination. No past medical history, no medications, and no alcohol or drug use.
Physical examination reveals a thin, ill-appearing young male in no acute distress.
T 36, P 100, BP 96/54, RR 16, SaO2 99% on room air
Head and neck examination is normal without nuchal rigidity.
Cardiac examination shows a regular tachycardia without murmurs.
Respiratory examination is clear.
Abdominal is benign.
Extremities are without cyanosis, clubbing, or edema.
Skin is without rashes.
Initial labs:
Na+ 138 mEq/L, K+ 3.2 mEq/L, Cl- 88 mEq/L, HCO3- 24 mEq/L, BUN 18 mg/dL, Cr 1.0 mg/dL, glucose 500 mg/dL
ABG: pH 7.40, pCO2 40 mmHg, pO2 112 mmHg
a. How would you characterize his acid-base status?
The patient is admitted to the hospital for new onset Type 1 diabetes mellitus. He is started on insulin therapy with improvement in his hyperglycemia over the next few hours but complains of muscle weakness and cramps. Repeat labs reveal:
Na+ 142 mEq/L, K+ 2.5 mEq/L, Cl- 100 mEq/L, HCO3- 22 mEq/L, BUN 12 mg/dL, Cr 0.9 mg/dL, glucose 200 mg/dL
b. List 5 contributing factors for his hypokalemia.
Anion gap metabolic acidosis or diabetic ketoacidosis with superimposed metabolic alkalosis. Although pH, CO2 and HCO3- are normal, the anion gap is 26 and the delta-delta is 14.
Hyperkalemia
1) Hyperaldosteronism from vomiting and volume depletion.
2) Insulin - Intracellular shifting
3) hyperadrenergic state from stress - intracellular shifting
4) Decreased intake from nausea and vomiting.
5) Increased urinary losses from polyuria.
Patient with Type I DM and poor medical compliance and develops hypertension and proteinuria. On a follow-up office visit, his blood pressure is 160/90. Labs reveal:
Na+ 134 mEq/L, K 5.0 mEq/L, Cl 100 mEq/L, HCO3 22 mEq/L, BUN 20 mg/dL, Cr 1.8 mg/dL, glucose 250 mg/dL, glycohemoglobin 9.0 (normal
Interventions
1) Tight glucose control.
2) Tight BP control.
3) ACEi/ARB
Anemia due to decreased EPO production
Pt w. 3-day hx of fatigue, weakness, and generalized malaise.
PMH: Type 2 DM, HTN, osteoarthritis and stage 2 chronic kidney disease with a baseline creatinine of 1.2 (estimated GFR 68 cc/min).
Rx: metoprolol, lisinopril, naproxen, and insulin.
A week ago, he developed fevers and a productive cough.
physical examination is remarkable for a temperature of 38.5, pulse 80 without orthostatic changes, blood pressure of 100/50 and diminished breath sounds in the right mid-lung field with egophony. Initial laboratory studies reveal;
Na+ 135 mEq/L, K+ 8.0 mEq/L, Cl- 100 mEq/L, HCO3- 18 mEq/L, BUN 100 mg/dL, Cr 6.2 mg/dL, glucose 340 mg/dL
Urine Na+ 22 mmol/L, Urine Cr 41 mg/dL
UA: pH 5, specific gravity 1.010, 1+ protein, trace glucose. Numerous muddy brown casts are seen on microscopy.
a. What is the NEXT STEP you should take in his evaluation?
b. List 5 potential causes for hyperkalemia in this patent.
c. Calculate his fractional excretion of sodium.
d. What is the most likely cause of his acute renal failure?
e. List 4 treatments that may be given for his hyperkalemia.
Get Electrocardiogram
Hyperkalemia
1) Acute renal failure (decreased filtration)
2) NSAID use
3) Metabolic acidosis / acidemia
4) Insulin deficiency
5) (Type IV RTA) – difficult to dx in advanced renal failure, but common in diabetic nephropathy
6) ACEI
7) Beta blockade
8) Hyperosmolarity from hyperglycemia (high serum glucose draws water out of cells, increasing intracellular K+ concentration; K+ leaves along its concentration gradient)
FENa = 2.46%
cause of his acute renal failure: Acute Tubular Necrosis. FENa > 2% is consistent with ATN.
Trmts:
1) Calcium
2) IV insulin and glucose
3) Albuterol
4) Kayexalate
5) Diuretics (any diuretic except K-sparing or acetazolamide)
6) Dialysis
7) Bicarbonate
Pt with creatinine is 5.5, on hospital day # 3 his creatinine is 4.6, and on hospital day # 4 his creatinine is 4.0. Can you accurately estimate his glomerular filtration rate or creatinine clearance on hospital day #3? Why or why not?
The GFR and creatinine clearance cannot be accurately estimated because he is not at steady-state.
AB status?
Na+ 140, K+ 4, Cl- 104, HCO3- 24
ABG: 7.40/40/100
No disorder; normal acid-base status. CO2, HCO3-, pH, anion gap are all normal.
AB status?
Na+ 140, K+ 4, Cl- 108, HCO3- 20
ABG: 7.33/38/100
Hyperchloremic metabolic acidosis. Anion gap is normal, CO2 is appropriate for this acidosis.
AB status?
Na+ 140, K+ 4, Cl- 90, HCO3- 16
ABG: 7.31/32/100
AG acidosis, metabolic alkalosis. Anion gap is elevated, CO2 is appropriate, but anion gap is up 22 and HCO3- is down only 8.
AB status?
Na+ 140, K+ 4, Cl- 110, HCO3- 12
ABG: 7.27/26/100
Hyperchloremic acidosis, AG acidosis. CO2 is again appropriate but anion gap is up 6 and HCO3- is down 12.
AB status?
Na+ 140, K+ 4, Cl- 112, HCO3- 16
ABG: 7.21/40/100
Hyperchloremic acidosis, respiratory acidosis. Normal anion gap acidosis with no evidence of respiratory compensation.
AB status?
Na+ 140, K+ 4, Cl- 109, HCO3- 19
ABG: 7.40/30/100
Hyperchloremic acidosis, respiratory alkalosis. Bicarbonate and CO2 are both down but pH is normal. Compensation should never be complete, therefore two primary disorders must be present.
76 yo M with diabetic nephropathy for routine followup. His serum creatinine has been gradually rising over the past 5 years and he is interested in pursuing hemodialysis if he develops ESRD. His past medical history includes hypertension and diabetes. He has never had surgery.
BP 150/90, P 80, R 16
Well nourished male in no distress.
HEENT examination is normal.
Cardiac examination reveals regular rate and rhythm without murmurs.
Respiratory examination is clear to auscultation and percussion.
Abdominal examination is benign.
Extremities are without cyanosis, clubbing, or edema.
Neurologic examination is normal.
Na+ 140, K+ 5.5, Cl- 106, HCO3- 18, BUN 40, Cr 2.5 (eGFR 27cc/min)
Ca++ 9.5, PO43- 6.8, PTH 128 (normal 35-70)
WBC 5.0, Hgb 9.2, Hct 30, Plt 200
Urine protein/Cr ratio 0.8
a. What is his stage of chronic kidney disease (CKD)?
b. What are his risk factors for CKD progression? What can be done to lower his risk of CKD progression?
c. Describe the relationship between his kidney disease and his laboratory abnormalities. 6
d. How would you treat this patient, and what would be your goals of therapy?
Stage IV
Risk Factors: Hypertension, diabetes, proteinuria, and age all increase his risk of CKD progression.
Lower risk by: reduced BP to
Definition of CKD
1) kidney damage for >3 mo, as evidenced by
- pathological changes
- markers of kidney damage (casts, hematuria, proteinuria)
- imaging studies
2) decr. GFR 3 mo
tests to run to confirm CKD?
urinary albumin:creatinine ratio
goal of treatment for CKD?
standard trmt for CKD? 4
Goal Treatment: slow progression of CKD and delay onset of ESRD
1) Bicarbonate (HCO3) for acidosis
2) ACEi for HTN
3) EPO for anemia
4) D vitamin for phosphate restriction
BEAD trmt for CKD
Pathogenesis of ∆Ca/PO4 metabolism and bone disease in CKD? 3 key steps
trmt? 2
CKD results in
- decr. Ca reabsorption -> incr. PTH levels -> incr. Ca/PO4 release from bone -> bone disease
- decr PO4 excretion -> incr. serum PO4 levels
- decr. 1,25OH production -> decr. GI uptake of Ca/PO4
trmt: 1,25-OH Vitamin D, and decrease PO4 intake.
4 features of nephrotic disease
4 features of nephritic disease
Name examples of each
Nephrotic "DAM Fine Man" PROTEINURIA Hypoalbuminemia Edema Hypercholesterolemia/Hyperlipidemia
Nephritic "Peeing Blood means Lupus" HEMATURIA Oliguria Azotemia (incr. urea, creatinine, nitrogen-rich compounds) HTN
Hematuric: Alport, Thin Membrane, IgA
